Exercise-Regulated Mitochondrial and Nuclear Signalling Networks in Skeletal Muscle

doi:10.1007/s40279-024-02007-2

Paper

Exercise-Regulated Mitochondrial and Nuclear Signalling Networks in Skeletal Muscle

Published Mar 25, 2024 · DOI · E. Reisman, John A. Hawley, Nolan J. Hoffman

Sports Medicine (Auckland, N.z.)

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Abstract

Exercise perturbs energy homeostasis in skeletal muscle and engages integrated cellular signalling networks to help meet the contraction-induced increases in skeletal muscle energy and oxygen demand. Investigating exercise-associated perturbations in skeletal muscle signalling networks has uncovered novel mechanisms by which exercise stimulates skeletal muscle mitochondrial biogenesis and promotes whole-body health and fitness. While acute exercise regulates a complex network of protein post-translational modifications (e.g. phosphorylation) in skeletal muscle, previous investigations of exercise signalling in human and rodent skeletal muscle have primarily focused on a select group of exercise-regulated protein kinases [i.e. 5ʹ adenosine monophosphate-activated protein kinase (AMPK), protein kinase A (PKA), Ca2+/calmodulin-dependent protein kinase (CaMK) and mitogen-activated protein kinase (MAPK)] and only a small subset of their respective protein substrates. Recently, global mass spectrometry-based phosphoproteomic approaches have helped unravel the extensive complexity and interconnection of exercise signalling pathways and kinases beyond this select group and phosphorylation and/or translocation of exercise-regulated mitochondrial and nuclear protein substrates. This review provides an overview of recent advances in our understanding of the molecular events associated with acute endurance exercise-regulated signalling pathways and kinases in skeletal muscle with a focus on phosphorylation. We critically appraise recent evidence highlighting the involvement of mitochondrial and nuclear protein phosphorylation and/or translocation in skeletal muscle adaptive responses to an acute bout of endurance exercise that ultimately stimulate mitochondrial biogenesis and contribute to exercise’s wider health and fitness benefits. Supplementary Information The online version contains supplementary material available at 10.1007/s40279-024-02007-2.

Literature Review

Study Snapshot

Exercise stimulates mitochondrial biogenesis and promotes overall health and fitness through complex skeletal muscle signaling networks.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

Exercise-Regulated Mitochondrial and Nuclear Signalling Networks in Skeletal Muscle

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